CNS Injury: Posttranslational Modification of the Tau Protein as a Biomarker

被引：11

作者：

Caprelli, Mitchell T. ^{[1
,2
]}

Mothe, Andrea J. ^{[2
]}

Tator, Charles H. ^{[1
,2
,3
]}

机构：

[1] Univ Toronto, Fac Med, Inst Med Sci, Toronto, ON, Canada

[2] Krembil Res Inst, Div Genet & Dev, Toronto, ON, Canada

[3] Univ Toronto, Div Neurosurg, Toronto, ON, Canada

来源：

NEUROSCIENTIST | 2019年 / 25卷 / 01期

关键词：

tau; biomarker; trauma; spinal cord injury; traumatic brain injury; concussion; TRAUMATIC BRAIN-INJURY; SPINAL-CORD-INJURY; GLYCOGEN-SYNTHASE KINASE-3-BETA; CEREBROSPINAL-FLUID; CLEAVED-TAU; ALZHEIMERS-DISEASE; AMYLOID-BETA; HYPERPHOSPHORYLATED TAU; PHOSPHORYLATED TAU; NEURONAL DAMAGE;

D O I：

10.1177/1073858417742125

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

The ideal biomarker for central nervous system (CNS) trauma in patients would be a molecular marker specific for injured nervous tissue that would provide a consistent and reliable assessment of the presence and severity of injury and the prognosis for recovery. One candidate biomarker is the protein tau, a microtubule-associated protein abundant in the axonal compartment of CNS neurons. Following axonal injury, tau becomes modified primarily by hyperphosphorylation of its various amino acid residues and cleavage into smaller fragments. These posttrauma products can leak into the cerebrospinal fluid or bloodstream and become candidate biomarkers of CNS injury. This review examines the primary molecular changes that tau undergoes following traumatic brain injury and spinal cord injury, and reviews the current literature in traumatic CNS biomarker research with a focus on the potential for hyperphosphorylated and cleaved tau as sensitive biomarkers of injury.

引用

页码：8 / 21

页数：14

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